Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pt > cholinergic antagonist > Flashcards

cholinergic antagonist Flashcards

1
Q

anticholinergics bind to the receptor and disrupt acetylcholine bind, so it is considered a ____________

A

competitive antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

antimuscarinic agents (atropine ) effect of muscarinic receptor blockade

A

Competitive antagonism at the muscarinic receptor (M1, M2 and M3)-mediated actions of acetylcholine on autonomic effectors innervated by postganglionic cholinergic nerves, as well as on smooth muscles that lack cholinergic innervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

antimuscarinic agents (atropine ) effect on ganglia

A

These agents have little effect on the actions of acetylcholine at the nicotinic receptor. E.g., autonomic ganglia (primarily involves ACh binding to nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

antimuscarinic agents (atropine ) effect on CNS

A

-Widespread distribution of muscarinic receptors throughout the brain
-Therapeutic doses are attributable to their central muscarinic blockade
-atropine can produce partial block (M1) only at relatively high doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

_____ is the oldest and most well known antimuscarinic agent that is an antagonist at M1, M2, and M3 receptors

A

atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

these agents are competitive antagonists for muscarinic receptors (M1, M2, and M3) ……..

A

smooth muscle
cardiac muscle
exocrine glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mechanisms of antimuscarinics agents

A

Competitive and reversible inhibition of muscarinic
receptor activation by preventing the binding of acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

two general classes of antimuscarinic

A

-tertiary amines: atropine (mainly used in ocular and CNS applications)
-quaternary amines: anisotropine (mainly used in GI tract and peripheral applications)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

tertiary amines

A

-good access to the CNS
-belladonna alkaloids (long acting)
-tertiary amines derivatives (short acting)
-tertiary amines derivatives (antiparkinson use)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

belladona alkaloids

A

atropine
scopolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

tertiary amine derivatives (short acting)

A

homatropine
tropicaminde

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

tertiary amine derivatives (antiparkinson use)

A

benztropine
trihexyphenidyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

quaternary amines

A

-derivatives of belladonna alkaloids
-ipratropium
-tiotropium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

long lasting tertiary amines

A

-M 1 /M 2 /M 3 non-selective
-Treat GI/urinary conditions, Motion sickness.
-Tertiary compounds therefore can affect the CNS
scopolamine has higher CNS penetration; induces greater drowsiness (low doses) or hallucinations (high doses).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

action of scopolamine (maldemar)

A

antimuscarinic with relatively more CNS action than atropine (highly lipophilic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

clinical use of scopolamine (maldemar)

A

effective treatment for motion sickness (oral or transdermal administration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

side effects of scopolamine (maldemar)

A

dry mouth
blurred vision
sedation
high dose: confusion and psychosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

short acting tertiary amines

A

-homatropine and tropicamine
-used in optical applications due to short duration of action cycloplegia and mydriasis
-homatropine is less toxic; tropicamide has a shorter duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

tertiary amines used for parkinsons disease

A

-benstropine
-have sedative activity
-used as an adjunct therapy with L-DOPA in PD patients (to achieve better balance between dopaminergic and cholinergic neurotransmission)
-Similar potency to atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

quaternary amines for COPD

A

atropine and ipratropium
-longer acting analog: tiotropium

21
Q

action of ipratropium

A

Antimuscarinic with receptor activity similar to atropine. M 3 antagonist blocks ACh-mediated constriction and open the airways

22
Q

clinical use of ipratropium

A

-Less effective as a monotherapy, but enhances the therapeutic effect of β-adrenergic agonists in COPD.
-COMBIVENT or DUONEB (trade name) – combination of ipratropium and albuterol effective in treating COPD

23
Q

problems of ipratropium

A

-few because of poor absorption
-toxic dose may cause hypotension (ganglionic blockade) and muscle weakness (neuromuscular blockade)

24
Q

Quaternary amines for GI disorders

A

-glycopyrrolate and propantheline bromide
-used to treat gastric disorders (GI spasms, peptic ulcers)
-glycopyrrolate: pre-op to reduce secretions (charged N makes crossing the gut difficult)

25
Q

antimuscarinics for overactive bladder (OAB)

A

tolterodine (detrol)
-newer M3 selective muscarinic antagonists (Fenacin) used to treat OAB
-advantages: lower incidence of constipation and confusion
-beta 3 receptor agonist (mirabegron)

26
Q

action of tolerodine

A

no apparent selectivity for different muscarinic receptor subtypes; however therapeutically seems to act somewhat selectively on M 3 receptor

27
Q

clinical use of tolterodine

A

overactive bladder

28
Q

problems of tolterodine

A

Still causes typical anticholinergic effects, but
significantly lower than with previous antimuscarinic drugs

29
Q

neuromuscular blocking drugs

A

look like ACh

30
Q

blocking the nicotinic receptor

A

-non depolarizing blockage (“normal” antagonist) tubocurarine
-depolarizing blockage (first activates, then blocks) succinylcholine

31
Q

effects nicotine on muscles: stimulation

A

-The normal operation of nicotinic receptors is the rapid degradation of synaptically released acetylcholine
-this allows the neuronal membrane or muscle endplate to repolarize and fast Na+ channels (responsible AP) to “reset”
-The next ACh release causes another depolarization which triggers the opening of the rested Na+ channel and AP

32
Q

effects nicotine on muscles: desensitization

A

-nicotinic receptors are specifically adapted to the transient nature of acetylcholine as a neurotransmitter

33
Q

non-depolarizing neuromuscular blocker

A

tubocurarine

34
Q

action of tubocurarine

A

nicotinic receptor competitive antagonist producing non-depolarizing blockade

35
Q

clinical use of tubocurarine

A

skeletal muscle relaxation during anesthesia- particularly useful for intubation

36
Q

problems of tubocurarine

A

minor

37
Q

depolarizing neuromuscular blocker

A

succinylcholine (SUX)

38
Q

action of succinylcholine

A

-Binds to nicotinic acetylcholine receptor
-Agonist nicotinic receptor, Initial depolarization (allows ion flow)
-Persistent depolarization makes the muscle fiber resistant to further stimulation by Ach (by preventing the “resetting” of voltage-gated sodium channels)
-Metabolized to choline by plasma Butyrylcholinesterase
-Slower than acetylcholinesterase
-Choline increase BP
-Muscle Fasciculation precedes paralysis
-Arm, neck, leg then respiratory muscles
Rapid onset (30-60 sec), short duration (5-10 min)

39
Q

clinical use of succinylcholine

A

-Skeletal muscle relaxation during anesthesia – particularly useful for intubation
-Also used for electro-convulsant therapy

40
Q

problem of succinylcholine

A
  • Muscle soreness; Avoid in hyperkalemia; cause of cardiac arrest
  • Malignant hyperthermia
  • prolonged paralysis can result in people with atypical plasma cholinesterases
41
Q

indirect acting: inhibition of ACh release

A

botulinum toxin

42
Q

action of botulinum toxin

A

inhibit release of acetylcholine

43
Q

clinical use of botulinum toxin

A

Dystonias (uncontollred muscle spasms), cerebral
palsy, spasm of ocular muscles, anal fissure, hyperhidrosis (excessive sweating)

44
Q

problems of botulinum toxin

A

spread from injection site

45
Q

ganglionic nicotinic receptor antagonist

A

hexamethinium

46
Q

action of hexamethonium

A

Antagonist at nicotinic receptors in autonomic ganglia thus blocking all SNS and PSNS activity

47
Q

clinical use of hexamethonium

A

-originally developed to treat hypertension but not used clinically due to adverse effects
-Good for teaching students about the ANS

48
Q

problems of hexamethonium

A

Blocking basal tone of SNS and PSNS resulting in:
* Blood vessels (SNS): hypotension
* Sweat glands (SNS): decreased perspiration
* Other glands (PSNS): dry mouth, decreased secretions
* Heart rate (PSNS): tachycardia (usually but sometimes if SNS active, will see bradycardia)
* Eye (PSNS): pupillary dilation and blurred vision
* Gut (PSNS): decreased tone and motility, constipation
* Bladder (PSNS): urinary retention

pt (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions